Stress, stress resistance and ageing

Normal ageing results from the imbalance between cellular damage, accrued throughout life, and the progressive decline in stress response and repair pathways. Reactive oxygen species (ROS) arising from a lifetime of mitochondrial respiration can damage DNA, protein or lipids and protein damage can in turn activate ER stress pathways.

Oxidative damage is a major causal factor in the physiological declines associated with normal ageing. At the cellular level oxidative damage can drive senescence, limiting proliferative competence and undermining processes such as tissue homeostasis and wound repair in old age.

Reactive Oxygen Species damage

ROS damage activates an array of stress responsive signalling pathways that coordinate the cell’s response to damage by: (i) initiating cell cycle arrest (so that damaged DNA is not propagated in daughter cells); (ii) driving the expression of detoxifying enzymes and chaperones; (iii) coordinating changes in protein synthesis and turnover/autophagy and (iv) in the most extreme cases eliciting cell death.

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